Alzheimer's Disease

Alzheimer's disease is a progressive brain disease causing severe mental deterioration (Gale, 2001). It is found most often in the elderly. Approximately 10 percent of people over age 65 and 40 percent to 50 percent of people over age 85 will get Alzheimer's. The disease is seen occasionally in people in their 30s and 40s. A positive diagnosis of Alzheimer's requires a brain biopsy, so it is usually not diagnosed until after death. The brains of Alzheimer's patients show atrophy of the neocortex. The hippocampus is also affected. Much of the shrinkage of the brain in these patients occurs in areas responsible for forming memories.

The brains of Alzheimer's patients contain amyloid plaques and tangles of neurofibrils (Gale, 2001). Although the neurofibrillary tangles are not unique to Alzheimer's, the severity of mental impairment correlates with loss of synaptic connections between brain cells, followed by the formation of neurofibrillary tangles. Amyloid plaques are found in the brains of normal people, but occur in much larger numbers in the brains of Alzheimer's patients. Neurotransmitters are found in lower concentrations in the brains of Alzheimer's patients.

The first symptoms of Alzheimer's disease is memory loss for recent events, which is much more severe than that normally occurring with advancing age (Gale, 2001). Patients with Alzheimer's disease may remain physically healthy, the mental decline continues, and later symptoms include disorientatio

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sease. The goal of research into Alzheimer's disease is to prevent the loss of synapses and neurons in the areas of the brain responsible for memory and cognition (Growdon, The Search 2002). Acetylcholinesterase inhibitors currently used to treat the cognitive symptoms of Alzheimer's disease temporarily compensate for the loss of nerve cells, but don't treat the underlying cause. Antiamyloid drugs and antioxidants are two promising strategies currently being explored. These drugs are hoped to target the cause of the central loss of synapses and neurons. Antiamyloid drugs would block the formation of beta-amyloid, the substance of amyloid plaques, which may be responsible for initiating the events leading to Alzheimer's disease, and believed to be toxic to neurons. In the production of beta-amylase, an enzyme called alpha-secretase cuts the protein in half into nontoxic fragments. If there is overactivation of two other enzymes, beta-secretase and gamma-secretase, a shorter, stickier protein, beta-amyloid, is formed. Current research is trying to develop drugs which either stimulate alpha-secretase, or inhibit beta- and gamma-secretase. Antioxidants could reduce the damage to neurons from free radicals (Growdon, The Se

Category: Medical - A